| Abstract: |
Macrophage infiltration, apoptosis, and lipid deposition greatly contribute to plaque vulnerability. Nuclear imaging provides at least two potential indicators to identify vulnerable plaques: F-18-fluorodeoxyglucose (FDG) as a marker of intraplaque inflammation and Tc-99m-annexin A5 as a marker of apoptosis. In this article we summarize our recent study on the comparison of F-18-FDG and Tc-99m-annexin A5 uptake in atherosclerotic lesions of the apolipoprotein E knockout (ApoE-/-) mouse, and briefly review previous studies on molecular imaging of atherosclerotic plaques using F-18-FDG and Tc-99m-annexin A5. The intralesional distribution of F-18-FDG and Tc-99m-annexin A5 was determined in male ApoE-/- mice. The mice were maintained on a high-fat diet after the age of 5 weeks. At 25 weeks, F-18-FDG or Tc-99m-annexin A5 was injected and the aortas were harvested. Regional radioactivity distribution was compared in relation to Oil Red O staining. Both F-18-FDG and Tc-99m-annexin A5 showed preferential uptakes into atherosclerotic lesions, with higher uptake levels for F-18-FDG than Tc-99m-annexin A5. The regional uptake levels of these tracers were significantly correlated with the Oil Red O staining score. The uptake ratios of advanced lesions to early lesions were significantly higher for Tc-99m-annexin A5 than for F-18-FDG. Previous studies have indicated that F-18-FDG and Tc-99m-annexin A5 are useful for the detection of vulnerable atherosclerotic lesions. Our findings could further characterize these tracers as follows: the high aortic uptake level of F-18-FDG may offer higher sensitivity in lesion detection, whereas the preferential uptake of Tc-99m-annexin A5 in advanced lesions suggests its potential for assessing the vulnerability of atherosclerotic plaques. |
